Prediction of dilutional acidosis based on the revised classical dilution concept for bicarbonate

Abstract

Due to the controversy surrounding the term dilutional acidosis, the classical dilution concept for bicarbonate has been rigorously revised for the prediction of pH, actual bicarbonate concentration, and base excess. In the algorithms derived for buffer solutions, blood, and whole body (1-, 2-, and 3-fluid compartment), only bicarbonate is considered. On dilution at constant Pco2, the final concentration of bicarbonate is the sum in terms of pH, due to the following processes: dilution, formation from chemical reaction with the nonbicarbonate buffers phosphate, hemoglobin, and plasma proteins, and transfer from erythrocytes and interstitial fluid to plasma. At constant Pco2, the level of carbonic acid is held constant, whereas those of the buffer bases are reduced by dilution, resulting in acidosis. In mixed bicarbonate/phosphate buffer, the final concentration of HCO3− exceeds the diluted value due to additional buffering of H2CO3 by HPO42−. For whole blood in vitro, pH, and actual bicarbonate concentration are predicted from dilution with 0.9% saline from initial Hb (100%) to infinite dilution (pure saline). The acidosis from dilution of plasma bicarbonate is mitigated by contributions from plasma proteins (<1 mmol/l) and from the erythrocytes (∼5 mmol/l). Similarly, for whole body, the main contributions to combat primary dilutional acidosis in the range of hemodilution (relative Hb: 100–50%) are from the erythrocytes (1.2–2.2 mmol/l) and from the interstitial fluid (3.3–7.2 mmol/l). Perioperatively measured nonrespiratory acidosis is predictable if caused by hemodilution with fluids containing neither bicarbonate nor its precursors, irrespective of other electrolytes.